PCGF5 is required for neural differentiation of embryonic stem cells

Mingze Yao, Xueke Zhou, Jiajian Zhou, Shixin Gong, Gongcheng Hu, Jiao Li, Kaimeng Huang, Ping Lai, Guang Shi, Andrew P. Hutchins, Hao Sun, Huating Wang and Hongjie Yao ()
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Mingze Yao: Guangzhou Medical University
Xueke Zhou: Guangzhou Medical University
Jiajian Zhou: the Chinese University of Hong Kong
Shixin Gong: Guangzhou Medical University
Gongcheng Hu: Guangzhou Medical University
Jiao Li: Guangzhou Medical University
Kaimeng Huang: Guangzhou Medical University
Ping Lai: Guangzhou Medical University
Guang Shi: Guangzhou Medical University
Andrew P. Hutchins: Southern University of Science and Technology
Hao Sun: the Chinese University of Hong Kong
Huating Wang: the Chinese University of Hong Kong
Hongjie Yao: Guangzhou Medical University

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract Polycomb repressive complex 1 (PRC1) is an important regulator of gene expression and development. PRC1 contains the E3 ligases RING1A/B, which monoubiquitinate lysine 119 at histone H2A (H2AK119ub1), and has been sub-classified into six major complexes based on the presence of a PCGF subunit. Here, we report that PCGF5, one of six PCGF paralogs, is an important requirement in the differentiation of mouse embryonic stem cells (mESCs) towards a neural cell fate. Although PCGF5 is not required for mESC self-renewal, its loss blocks mESC neural differentiation by activating the SMAD2/TGF-β signaling pathway. PCGF5 loss-of-function impairs the reduction of H2AK119ub1 and H3K27me3 around neural specific genes and keeps them repressed. Our results suggest that PCGF5 might function as both a repressor for SMAD2/TGF-β signaling pathway and a facilitator for neural differentiation. Together, our findings reveal a critical context-specific function for PCGF5 in directing PRC1 to control cell fate.

Date: 2018
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DOI: 10.1038/s41467-018-03781-0

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